Trigeminal Injury Research Articles

Trigeminal nerve injuries following dental procedures: A retrospective analysis of malpractice claims from 2016 to 2023 in South Korea

BackgroundDental malpractice claims, which pertain to legal actions against dentists accused of clinical negligence that caused harm to patients, have increased in the past ten years in South Korea. The claims are caused by complications, particularly trigeminal nerve injuries, resulting from various dental procedures. Medicolegal issues related to trigeminal nerve injury have not been previously described in South Korea. Therefore, in this study, we aimed to identify the general, dental, and judicial characteristics of closed dental malpractice claims. MethodsThis study was designed as a descriptive study. We collected the data of 51 closed claims related to trigeminal nerve injury resulting from dental procedures such as dental implant emplacement, tooth extraction, and local anesthesia. The claims were decided by courts in South Korea between 2016 and 2023. The general, dental, and judicial characteristics of the claims were analyzed retrospectively. ResultsThe average claim resolution period was 4.2 (range: 1.47–8.39) years post-adverse events that occurred more frequently in dental clinics (68.6 %) than in dental (25.5 %) or general hospitals (5.9 %). Inferior alveolar (66.7 %) and lingual (17.6 %) nerves were injured following dental procedures. The duty to inform was breached in 68.6 % of claims. The dental procedure performed (P < 0.001) and the injured nerve (P < 0.001) were associated with the violation of the duty to care. ConclusionTo improve the quality of dental care services, the analysis of the adverse events using various resources including judgments should be strongly addressed.

Central vein sign and trigeminal lesions of multiple sclerosis visualised by 7T MRI

BackgroundAlthough trigeminal nerve involvement is a characteristic of multiple sclerosis (MS), its prevalence across studies varies greatly due to MRI resolution and cohort selection bias. The mechanism behind the site...

MicroRNA-6954-3p Downregulation Contributes to Orofacial Neuropathic Pain in Mice Via Targeting Voltage-Gated Sodium Channel β2 Subunit Protein

The voltage-gated sodium channel β2 subunit protein (SCN2B) plays a crucial role in neuropathic pain. However, the role and mechanisms of SCN2B in orofacial neuropathic pain are still unclear. This study aimed to investigate the upstream regulatory mechanisms of SCN2B in the trigeminal ganglion (TG) underlying orofacial neuropathic pain. Chronic constriction injury of the infraorbital nerve (CCI-ION) of mice was performed to establish the model of orofacial neuropathic pain. Von Frey filament test was performed to detect the head withdrawal threshold (HWT) of mice. Quantitative reverse transcription-polymerase chain, western blotting (WB), fluorescence in situ hybridization, and immunofluorescence (IF) staining were used to detect the expression and distribution of SCN2B and miR-6954-3p in the TG of mice. A luciferase activity assay was carried out to prove the binding between SCN2B messenger ribonucleic acid (mRNA) and miR-6954-3p. After the CCI-ION surgery, the levels of Scn2b mRNA and protein significantly increased and miR-6954-3p decreased in the TG of mice with decreasing HWT. IF staining revealed that SCN2B was expressed specifically in the TG neurons. Silencing SCN2B in the TG of CCI-ION mice significantly increased the HWT. Importantly, the 3′-untranslated region of Scn2b mRNA was proved to bind with miR-6954-3p. Fluorescence in situ hybridization and IF staining demonstrated that miR-6954-3p was expressed in TG neurons and co-expressed with SCN2B. Furthermore, intraganglionic injection of miR-6954-3p agomir into the TG of CCI-ION mice resulted in the downregulation of SCN2B and increased the HWT. These findings suggest that the downregulation of miR-6954-3p in the TG promotes orofacial neuropathic pain by promoting SCN2B expression following trigeminal nerve injury. PerspectiveThis study points to the important role of SCN2B in orofacial neuropathic pain. Furthermore, miR-6954-3p is proven to regulate the expression of SCN2B by binding to the 3′-untranslated region of Scn2b mRNA. These findings indicate that SCN2B and miR-6954-3p are potential therapeutic targets for the treatment of orofacial neuropathic pain.

Pharmacologic management of trigeminal nerve injury after endodontic treatment: A retrospective analysis.

Trigeminal nerve injury following endodontic treatment, leading to unpleasant sensations or partial sensory loss in the face or oral mucosa, is uncommon but significant when it occurs. This study analysed the pharmacological management of trigeminal nerve injuries (TNI) in a university-based hospital. We conducted a retrospective analysis of 47 patients who visited the Department of Orofacial Pain and Oral Medicine at Yonsei University Dental Hospital, Seoul, Korea, after TNI following endodontic procedures in primary clinics. Both objective tests and subjective evaluations, assessed the extent and duration of sensory injury during the initial visit. The patient's initial symptoms, presumed cause of TNI, referral delay (time interval between TNI and the first visit to our clinic), and medications were analysed to determine whether these factors affected the outcomes. Most patients with TNI experienced dysesthesia with hypoesthesia (70.2%). The mandibular molars were predominantly affected (72.3%), with the inferior alveolar nerve (IAN), lingual nerve (LN), both IAN and LN, and maxillary nerve compromised in 83.0, 12.8, 2.1, and 2.1% of cases, respectively. Causes of TNI included local anaesthesia (29.8%), overfilling/over-instrumentation (25.5%), endodontic surgery (17.0%), and unknown factors (27.7%). A shorter referral delay was associated with better outcomes, with an average delay of 8.6 weeks for symptom improvement compared with 44.1 weeks for no change. The medication regimens included steroids, NSAIDs, topical lidocaine, vitamin B complex, Adenosine Triphosphate (ATP), antiepileptics, antidepressants, and opioids administered alone or in combination, with a mean duration of 20.7 weeks. 53.2% of the patients reported improvement in their symptoms, 27.7% experienced no significant change, and 19.1% had unknown outcomes. Swift referral to an orofacial pain specialist is recommended for effective recovery in cases of TNI arising from endodontic treatment.

Foxg1 Modulation of the Prkcd Gene in the Lateral Habenula Mediates Trigeminal Neuralgia-Associated Anxiety-Like Behaviors in Mice.

Trigeminal Neuralgia (TN) is a debilitating disorder frequently accompanied by mood complications such as depression and anxiety. The current study sought to elucidate the molecular underpinnings that contribute to the pathogenesis of TN and its associated anxiety. Employing a partial transection of the infraorbital nerve (pT-ION) in a murine model, we successfully induced sustained primary and secondary orofacial allodynia alongside anxiety-like behavioral manifestations. Transcriptome-wide gene microarray analyses revealed a marked upregulation of Foxg1 subsequent to pT-ION. Targeted knockdown of Foxg1, achieved through bilateral microinjection of adeno-associated virus harboring Foxg1-specific shRNA into the lateral habenula (LHb), resulted in a significant attenuation of both orofacial pain and anxiety-like behaviors. Subsequent RNA sequencing implicated Prkcd as a downstream effector gene modulated by Foxg1. Pharmacological inhibition of protein kinase C delta, encoded by Prkcd, within the LHb markedly ameliorated pT-ION-induced symptomatology. The dual luciferase assay revealed that Foxg1 substantially enhances the transcriptional activity of the Prkcd gene. Collectively, these findings indicate that trigeminal nerve injury leads to Foxg1 upregulation in the LHb, which in turn elevates the expression of Prkcd, culminating in the manifestation of orofacial pain and anxiety-like behaviors. This work offers promising therapeutic targets and a conceptual framework for the clinical management of TN and its psychological comorbidities.

Accuracy of MR neurography as a diagnostic tool in detecting injuries to the lingual and inferior alveolar nerve in patients with iatrogenic post-traumatic trigeminal neuropathy

ObjectivesMR neurography has the ability to detect and depict peripheral nerve injuries. This study evaluated the potential of MR neurography in the diagnosis of post-traumatic trigeminal neuropathy.MethodsForty-one participants prospectively underwent MR neurography of the lingual and inferior alveolar nerves using a 3D TSE STIR black-blood sequence. Two blinded and independent observers recorded the following information for each nerve of interest: presence of injury, nerve thickness, nerve signal intensity, MR neurography Sunderland class, and signal gap. Afterwards, the apparent nerve-muscle contrast-to-noise ratio and apparent signal-to-noise ratio were calculated. Clinical data (neurosensory testing score and clinical Sunderland class) was extracted retrospectively from the medical records of patients diagnosed with post-traumatic trigeminal neuropathy.ResultsCompared to neurosensory testing, MR neurography had a sensitivity of 38.2% and specificity of 93.5% detecting nerve injuries. When differentiated according to clinical Sunderland class, sensitivity was 19.1% in the presence of a low class injury (I to III) and improved to 83.3% in the presence of a high class (IV to V). Specificity remained unchanged. The area under the curve using the apparent nerve-muscle contrast-to-noise ratio, apparent signal-to-noise ratio, and nerve thickness to predict the presence of an injury was 0.78 (p < .05). Signal intensities and nerve diameter increased in injured nerves (p < .05). Clinical and MR neurography Sunderland scores positively correlated (correlation coefficient = 0.53; p = .005).ConclusionsThis study shows that MR neurography can accurately differentiate between injured and healthy nerves, especially in the presence of a more severe nerve injury.Clinical relevance statementMR neurography is not only able to detect trigeminal nerve injuries, but it can also provide information about the anatomical specifications of the injury, which is not possible with clinical neurosensory testing. This makes MR neurography an added value in the management of post-traumatic trigeminal neuropathy.Key Points• The current diagnosis of post-traumatic trigeminal neuropathy is mainly based on clinical examination.• MR neurography is able to visualize and stratify peripheral trigeminal nerve injuries.• MR neurography contributes to the diagnostic process as well as to further decision-making.

Involvement of interferon gamma signaling in spinal trigeminal caudal subnucleus astrocyte in orofacial neuropathic pain in rats with infraorbital nerve injury.

Background: Trigeminal nerve injury causes orofacial pain that can interfere with activities of daily life. However, the underlying mechanism remains unknown, and the appropriate treatment has not been established yet. This study aimed to examine the involvement of interferon gamma (IFN-γ) signaling in the spinal trigeminal caudal subnucleus (Vc) in orofacial neuropathic pain. Methods: Infraorbital nerve (ION) injury (IONI) was performed in rats by partial ION ligation. The head-withdrawal reflex threshold (HWT) to mechanical stimulation of the whisker pad skin was measured in IONI or sham rats, as well as following a continuous intracisterna magna administration of IFN-γ and a mixture of IFN-γ and fluorocitrate (inhibitor of astrocytes activation) in naïve rats, or an IFN-γ antagonist in IONI rats. The IFN-γ receptor immunohistochemistry and IFN-γ Western blotting were analyzed in the Vc after IONI or sham treatment. The glial fibrillary acid protein (GFAP) immunohistochemistry and Western blotting were also analyzed after administration of IFN-γ and the mixture of IFN-γ and fluorocitrate. Moreover, the change in single neuronal activity in the Vc was examined in the IONI, sham, and IONI group administered IFN-γ antagonist. Results: The HWT decreased after IONI. The IFN-γ and IFN-γ receptor were upregulated after IONI, and the IFN-γ receptor was expressed in Vc astrocytes. IFN-γ administration decreased the HWT, whereas the mixture of IFN-γ and fluorocitrate recovered the decrement of HWT. IFN-γ administration upregulated GFAP expression, while the mixture of IFN-γ and fluorocitrate recovered the upregulation of GFAP expression. IONI significantly enhanced the neuronal activity of the mechanical-evoked responses, and administration of an IFN-γ antagonist significantly inhibited these enhancements. Conclusions: IFN-γ signaling through the receptor in astrocytes is a key mechanism underlying orofacial neuropathic pain associated with trigeminal nerve injury. These findings will aid in the development of therapeutics for orofacial neuropathic pain.

Phosphorylation of the AMPARs regulated by protein kinase C (PKC) and protein interacting with C-kinase 1 (PICK1) contribute to orofacial neuropathic pain

The α-amino-3-hydroxy-5-methylisoxazole-4-isoxazolepropionic acid receptor (AMPAR) has been recognized to play a vital role in the development of neuropathic pain. Recent studies have indicated that protein kinase C (PKC) and protein interacting with C-kinase 1 (PICK1) are involved in the phosphorylation of AMPARs. However, whether PKC and PICK1 were involved in the AMPAR phosphorylation in the trigeminal ganglion (TG) to participate in orofacial neuropathic pain remains enigmatic. A behavioral test was utilized to evaluate the head withdrawal threshold (HWT) after chronic constriction injury of the infraorbital nerve (CCI-ION). The distribution and expression of GluA1, GluA2, PKC, and PICK1 were examined in the trigeminal ganglion (TG) by immunofluorescence, real-time reverse transcription-quantitative polymerase chain reaction, immunoblotting, and co-immunoprecipitation. Intra-ganglionic injections of drugs were performed to investigate the regulation mechanism. The present study demonstrated that CCI-ION-induced mechanical allodynia was maintained over at least 21 days. GluA1 and GluA2 were mainly expressed in the neurons. Trigeminal nerve injury potentiated the phosphorylation of GluA1, GluA2, and PKC in the TG, which was prevented by inhibiting PKC with chelerythrine chloride. Additionally, PICK1 colocalized and interacted with GluA2 in the TG. Following blocking PICK1 with FSC-231, the phosphorylation of GluA2 decreased. Finally, inhibition of PKC and PICK1 both alleviated mechanical allodynia in the whisker pad of CCI-ION mice. In conclusion, activation of PKC and PICK1 contribute to orofacial allodynia by regulating AMPAR phosphorylation in the TG of male mice, which provides potential therapeutic targets for alleviating orofacial neuropathic pain.

Trigeminal Neuralgia as a Primary Demyelinating Disease: Potential Multimodal Evidence and Remaining Controversies

Trigeminal neuralgia is a heterogeneous disorder with likely multifactorial and complex etiology; however, trigeminal nerve demyelination and injury are observed in almost all patients with trigeminal neuralgia. The current management strategies for trigeminal neuralgia primarily involve anticonvulsants and surgical interventions, neither of which directly address demyelination, the pathological hallmark of trigeminal neuralgia, and treatments targeting demyelination are not available. Demyelination of the trigeminal nerve has been historically considered a secondary effect of vascular compression, and as a result, trigeminal neuralgia is not recognized nor treated as a primary demyelinating disorder. In this article, we review the evolution of our understanding of trigeminal neuralgia and provide evidence to propose its potential categorization, at least in some cases, as a primary demyelinating disease by discussing its course and similarities to multiple sclerosis, the most prevalent central nervous system demyelinating disorder. This proposed categorization may provide a basis in investigating novel treatment modalities beyond the current medical and surgical interventions, emphasizing the need for further research into demyelination of the trigeminal sensory pathway in trigeminal neuralgia. PerspectiveThis article proposes trigeminal neuralgia as a demyelinating disease, supported by histological, clinical, and radiological evidence. Such categorization offers a plausible explanation for controversies surrounding trigeminal neuralgia. This perspective holds potential for future research and developing therapeutics targeting demyelination in the condition.

Pathophysiology, Clinical Implications and Management of Orofacial Neuropathic Pain- with special attention to Trigeminal neuralgia: A Narrative Review

Background: It is a widely held belief that if the trigeminal nerve is damaged, the victim would experience agonising and unrelenting external pain. A lesion to the trigeminal nerve may have a wide-reaching effect, such as on one side of the face in particular, or it might have a more localised effect, such as on some or all of your gums. The risk of damage increases the likelihood that it will be difficult to speak and swallow. This nerve provides sensation to a part of your face that may be constantly aching or tingling for some people. However, the trigeminal nerve injury-related persistent orofacial pain might be brought on by a wide variety of unknown triggers. Aim: In this study investigate the clinical manifestations of chronic orofacial pain brought on by a damage to the trigeminal nerve, as well as the diagnostic and therapeutic approaches available to treat this condition. Methodology Through the use of search phrases such as "Trigeminal nerve injury," "Trigeminal ganglion," "Trigeminal spinal subnucleus caudalis," "Craniofacial pain," "Oral prognosis," and "treatment," the computerised databases for the last twenty years have been investigated. There are now two hundred objects in total that have been accumulated. There have been around fifty of them that are pertinent to the discussion that is going on in this work. Majority of the patients fair enough with the pharmacology treatment/drugs like the carbamazepine &amp; oxcarbazepine which forms the first line treatment options followed by lamotrigine &amp; baclofen encompassing the second line of drugs along with adjuvant drug support of topiramate, levetiracetam, gabapentin, pregabalin. As the field of science has explored &amp;advanced for the latest treatment options include microvascular decompression, gamma knife radiosurgery, percutaneous rhizotomies variable based on the evidences &amp; guidelines 54 Conclusion: New diagnostic criteria and treatment alternatives have become available for people who suffer from trigeminal neuropathy and orofacial neuropathic pain as a result of recent developments in fundamental animal research that have led to their development. Despite the results, more research needs to investigate a greater variety of distinct non-neuronal cell feature approaches.

Patterns of Third-Molar-Pericoronitis-Related Pain: A Morphometrical Observational Retrospective Study.

Mandibular third molar (M3M) removal and the management of postoperative complications represent a common matter of interest in oral and maxillofacial surgery. Pain represents a great symptom for patients affected by pericoronitis and it is the most common indication for third molar removal. The aim of the present article is to search for patterns of pre-operative pain in patients before undergoing third molar surgery and to test for a relation between some patterns of symptoms, such as pain intensity, site of symptomatic tooth, and referred area of pain. This retrospective observational study enrolled a total of 86 patients, aged (mean ± SD) 34.54 ± 13.62 years (range 17-78 years), scheduled for outpatient third molar extraction at the Oral Surgery School, Department of Medical Biotechnologies, Policlinico "Le Scotte", University of Siena. Pericoronitis and pain were the symptoms of the patients and the indication of extraction. Inclusion criteria were the presence of partially impacted third molars, confirmed with a preoperative panoramic radiograph, and preoperative pain. Exclusion criteria were known neurological disease (such as previous trigeminal or facial nerve injuries), impaired communicative or cognitive disease, diagnosed diabetes mellitus, and oral surgical intervention within 30 days before data collection. Patients were visited and asked to answer a morphometric analytic questionnaire about their perception of pain referred to the third molar. Analyses were performed on statistical evaluation on age, age ranges, patient gender, prior third molar extraction, site of pericoronitis, pain score (1-10), and pain area. Two-tailed p values of less than 0.05 were considered significant if not otherwise specified. No correlations were found between age, gender, previous extraction, tooth site (maxillar on mandible), pain score, and pain area. Patterns of third molar pericoronitis pain among 86 patients were reported. A significant correlation was found between pain score and pain area (p = 0.0111, rs = 0.3131). Pain intensity has indeed some kind of responsibility in determining the orofacial distribution of pain. The pain area referral patterns of the present article could be considered as a pain model resulting from the pericoronitis of maxillar and mandibular third molars.

Consensus guidelines on training, diagnosis, treatment and follow-up care of trigeminal nerve injuries

The aim was to present expert-based guidelines on the management of trigeminal nerve injuries. A two-round multidisciplinary Delphi study was conducted amongst international trigeminal nerve injury experts with a set of statements and three summary flowcharts using a nine-point Likert scale (1 = strongly disagree; 9 = strongly agree). An item was deemed appropriate if the median panel score was within the range of 7–9, undecided if the score was 4–6, and inappropriate if the score was 1–3. Consensus was achieved if at least 75% of panelists scored within one range. Eighteen specialists from dental, medical, and surgical specialties participated in both rounds. Consensus was reached on most statements related to training/services (78%) and diagnosis (80%). Statements related to treatment were mainly undecided due to a lack of sufficient evidence for some of the proposed treatments. Nevertheless, the summary treatment flowchart reached consensus with a median score of eight. Recommendations on follow-up and opportunities for future research were discussed. None of the statements were deemed inappropriate. A set of recommendations and accepted flowcharts are presented; these will aid professionals involved in managing patients with trigeminal nerve injuries.

The mTOR inhibitor rapamycin suppresses trigeminal neuropathic pain and p-MKK4/p-p38 mitogen-activated protein kinase-mediated microglial activation in the trigeminal nucleus caudalis of mice with infraorbital nerve injury.

Neuropathic pain caused by trigeminal nerve injury is a typical refractory orofacial chronic pain accompanied by the development of hyperalgesia and allodynia. We previously demonstrated that the mammalian target of rapamycin (mTOR) inhibitor rapamycin suppressed orofacial formalin injection-induced nociception; however, the underlying mechanism is unclear, and it is unknown whether it can reduce trigeminal neuropathic pain. In mice, left infraorbital nerve and partial nerve ligation (ION-pNL) was performed using a silk suture (8-0). Fourteen days after surgery, neuropathic pain behavior was examined on a whisker pad and rapamycin (0.1, 0.3, and 1.0 mg/kg) was administered intraperitoneally. Mechanical and cold sensitivities in the orofacial region were quantified using von Frey filaments and acetone solution, respectively. Changes in mTOR and related proteins, such as p-MKK3/6, p-MKK4, p-JNK, p-ERK, p-p38 MAPK, GFAP, and Iba-1, in the trigeminal nucleus caudalis (TNC) or the trigeminal ganglia (TG) tissues were examined via western blot analysis or immunohistochemistry. Mice demonstrated significant mechanical and cold allodynia 2 weeks following ION-pNL injury, both of which were significantly reduced 1 h after the administration of high-dose rapamycin (1.0 mg/kg). In the TG tissue, ION-pNL surgery or rapamycin treatment did not change p-mTOR and p-4EBP1, but rapamycin reduced the increase of p-S6 and S6 induced by ION-pNL. In the TNC tissue, neither ION-pNL surgery nor rapamycin treatment altered p-mTOR, p-S6, and p-4EBP1 expressions, whereas rapamycin significantly decreased the ION-pNL-induced increase in Iba-1 expression. In addition, rapamycin suppressed the increase in p-p38 MAPK and p-MKK4 expressions but not p-MKK3/6 expression. Moreover, p-p38 MAPK-positive cells were colocalized with increased Iba-1 in the TNC. Our findings indicate that rapamycin treatment reduces both mechanical and cold orofacial allodynia in mice with trigeminal neuropathic pain, which is closely associated with the modulation of p-MKK4/p-p38 MAPK-mediated microglial activation in the TNC.

Identification Of The Afferent Subpopulation(S) In Which NaV1.1 Is Upregulated Following Trigeminal Nerve Injury

Identification Of The Afferent Subpopulation(S) In Which NaV1.1 Is Upregulated Following Trigeminal Nerve Injury

What are the Effects of Internal Fixation on Trigeminal Neurosensory Function and the Temporomandibular Joints Following Intraoral Vertical Ramus Osteotomy?

Intraoral vertical ramus osteotomy (IVRO) has, traditionally, been accomplished without internal fixation, necessitating a period of maxillomandibular fixation (MMF). With advances in instrumentation, internal fixation of IVRO is feasible, obviating the need for MMF. The purpose is to investigate the effects of transoral internal fixation on the prevalence of third division trigeminal nerve (CNV3) injury, temporomandibular joint (TMJ) arthralgia, and surgical site bleeding following IVRO. A retrospective study was conducted on patients who underwent IVRO at Vanderbilt University Medical Center between January 2017 and December 2020. The primary predictor variable was fixation status-internal fixation versus MMF. The primary outcome variable was postoperative CNV3 neurosensory disturbance. The secondary outcome variables were TMJ arthralgia and surgical site bleeding. Statistical analysis included Fisher's exact test and McNemar's Chi-squared test. Seventy two subjects (59 IVROs without internal fixation and 65 IVROs with internal fixation) were studied. The frequency of CNV3 neurosensory deficit was 0% in the IVRO without internal fixation group and 3.1% in the IVRO with internal fixation group (P=.49). Within group analysis showed a decreased frequency of postoperative TMJ arthralgia compared to preoperative records in both groups (IVRO without internal fixation group, P=.04 and IVRO with internal fixation group, P=.004). The frequency of active surgical site bleeding controlled with local measures was 1.7% in the IVRO without internal fixation group and 3.1% in the IVRO with internal fixation group (P=1). Internal fixation of IVRO is associated with low incidence of neurosensory deficit, TMJ arthralgia, and active surgical site bleeding.

Transoral Endoscopic-Assisted Reduction and Internal Fixation of Mandibular Condylar Fractures in Children

Extraoral approaches for open reduction and fixation of condylar fractures in children are associated with serious risks of complications, including facial nerve injury, facial scarring, parotid fistula, and auriculotemporal nerve injury. The purpose of this study was to retrospectively evaluate the outcomes of transoral endoscopic-assisted open reduction and internal fixation of condylar fractures and hardware removal in pediatric patients. This study was designed as a retrospective case series. The study included pediatric patients admitted with condylar fractures that were indicated for treatment with open reduction and internal fixation. The patients were clinically and radiographically evaluated with regard to occlusion, mouth opening, lateral and protrusive movement of the mandible, pain, chewing and speech difficulties, and bone healing at the fracture site. CT images were used to assess the reduction of the fractured segment, the stability of fixation and progress of healing of the condylar fracture at follow-up visits. The same surgical treatment approach was applied to all patients. The data from the study were analyzed for a single group without any comparison to other groups. The technique was used for the treatment of 14 subcondylar fractures in 12 patients between the ages of 3 to 11years. A total of 28 transoral endoscopic-assisted approach to the condylar region either for reduction and internal fixation or hardware removal were applied. The mean operating time was 53.1 (±11.3) minutes for the fracture repair and 20 (±2.6) minutes for hardware removal, respectively. The mean follow-up time of the patients was 17.8 (±2.7) months (median: 18) months. All patients regained stable occlusion, satisfactory mandibular motion, stable fixation, and complete bone healing at the fracture site at the end of their follow-up period. There was no transient of permanent facial nerve or trigeminal nerve injury in any of the patients. Endoscopically assisted transoral approach is a reliable technique for reduction and internal fixation of condylar fracture and hardware removal in pediatric patients. The serious risks of extraoral approaches including facial nerve injury, facial scar, and parotid fistula can be eliminated by using this technique.

Glial cell line-derived neurotrophic factor and brain-derived neurotrophic factor regulate the interaction between astrocytes and Schwann cells at the trigeminal root entry zone.

The trigeminal root entry zone is the zone at which the myelination switches from peripheral Schwann cells to central oligodendrocytes. Its special anatomical and physiological structure renders it susceptible to nerve injury. The etiology of most primary trigeminal neuralgia is closely related to microvascular compression of the trigeminal root entry zone. This study aimed to develop an efficient in vitro model mimicking the glial environment of trigeminal root entry zone as a tool to investigate the effects of glial cell line-derived neurotrophic factor and brain-derived neurotrophic factor on the structural and functional integrity of trigeminal root entry zone and modulation of cellular interactions. Primary astrocytes and Schwann cells isolated from trigeminal root entry zone of postnatal rats were inoculated into a two-well silicon culture insert to mimic the trigeminal root entry zone microenvironment and treated with glial cell line-derived neurotrophic factor and brain-derived neurotrophic factor. In monoculture, glial cell line-derived neurotrophic factor promoted the migration of Schwann cells, but it did not have effects on the migration of astrocytes. In the co-culture system, glial cell line-derived neurotrophic factor promoted the bidirectional migration of astrocytes and Schwann cells. Brain-derived neurotrophic factor markedly promoted the activation and migration of astrocytes. However, in the co-culture system, brain-derived neurotrophic factor inhibited the migration of astrocytes and Schwann cells to a certain degree. These findings suggest that glial cell line-derived neurotrophic factor and brain-derived neurotrophic factor are involved in the regulation of the astrocyte-Schwann cell interaction in the co-culture system derived from the trigeminal root entry zone. This system can be used as a cell model to study the mechanism of glial dysregulation associated with trigeminal nerve injury and possible therapeutic interventions.

Trigeminal Trophic Syndrome.

Trigeminal trophic syndrome (TTS) is a rare cause of facial ulceration resulting from self-manipulation of skin following peripheral or central injury to the trigeminal system. The average period between the trigeminal nerve injury and the onset of ulcer varies from several weeks to many years.[1] The syndrome is characterized by a triad of anesthesia, paresthesia, and a secondary persistent or recurrent facial ulceration. The common dermatological causes are Hansen’s disease and herpes zoster.[2,3] Timely recognition of TTS will promote its correct diagnosis and better management. The condition has been reported to be associated with Alzheimer’s disease and meningioma.[4] We describe TTS in a 70-year-old male who was presented with a persistent linear ulcer on the forehead and severe scarring involving the forehead, upper eyelid, and left nose [Figure 1], following an episode of herpes zoster affecting the ophthalmic division of the trigeminal nerve 1 year ago.Figure 1: Linear ulcer on the forehead and scarring involving the forehead upper eyelid and left side of the noseDeclaration of patient consent The authors certify that they have obtained all appropriate patient consent forms. In the form, the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed. Financial support and sponsorship Nil. Conflicts of interest There are no conflicts of interest.

Pathophysiology of Post-Traumatic Trigeminal Neuropathic Pain

Trigeminal nerve injury is one of the causes of chronic orofacial pain. Patients suffering from this condition have a significantly reduced quality of life. The currently available management modalities are associated with limited success. This article reviews some of the common causes and clinical features associated with post-traumatic trigeminal neuropathic pain (PTNP). A cascade of events in the peripheral and central nervous system function is involved in the pathophysiology of pain following nerve injuries. Central and peripheral processes occur in tandem and may often be co-dependent. Due to the complexity of central mechanisms, only peripheral events contributing to the pathophysiology have been reviewed in this article. Future investigations will hopefully help gain insight into trigeminal-specific events in the pathophysiology of the development and maintenance of neuropathic pain secondary to nerve injury and enable the development of new therapeutic modalities.

Astrocytic and microglial interleukin-1β mediates complement C1q-triggered orofacial mechanical allodynia

Glial cells, such as microglia and astrocytes, in the trigeminal spinal subnucleus caudalis (Vc) are activated after trigeminal nerve injury and interact with Vc neurons to contribute to orofacial neuropathic pain. Complement C1q released from microglia has been reported to activate astrocytes and causes orofacial mechanical allodynia. However, how C1q-induced phenotypic alterations in Vc astrocytes are involved in orofacial pain remains to be elucidated. Intracisternal administration of C1q caused mechanical allodynia in the whisker pad skin and concurrent significant upregulation of glial fibrillary acidic protein and ionized calcium-binding adapter molecule 1 in the Vc. Immunohistochemical analyses clarified that C1q induces a significant increase in the cytokine interleukin (IL)-1β, predominantly in Vc astrocytes and partially in Vc microglia. The number of c-Fos-positive neurons in the Vc increased significantly in response to C1q. IL-1 receptor antagonist (IL-1Ra) was used to analyze the involvement of IL-1β in C1q-induced mechanical allodynia. Intracisternal administration of IL-1Ra ameliorated C1q-induced orofacial mechanical allodynia. The present findings suggest that IL-1β released from activated astrocytes and microglia in the Vc mediates C1q-induced orofacial pain.